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A unique reaction of mitomycin is the induction of microangiopathic hemolytic anemia Other Chemotherapeutic Agents/Newer concurrently with noncardiogenic pulmonary Antineoplastic Drugs edema and renal failure trusted 25 mg sominex. Other chemotherapeutic drugs are less com- The combination of mitomycin with vinca alka- monly associated with adverse pulmonary effects generic sominex 25mg with mastercard, loids (eg buy sominex 25mg free shipping, vinblastine and vincristine) induces an which are seen more often than with the agents acute onset ( 3 h after receiving the vinca alkaloid) reviewed earlier. Chlorambucil, which is an alkylat- of bronchospasm that is associated with focal or dif- ing agent similar to cyclophosphamide, is used in fuse interstitial infiltrates seen on chest radiographs the treatment of lymphoproliferative disorders as and hypoxemia. Fludarabine, an tive biological response modifier that induces antimetabolite that is used in the management of 330 Drug-Induced Lung Diseases (Kamp) patients with chronic lymphoproliferative disor- the development of opportunistic pulmonary ders, can cause chronic pneumonitis/fibrosis as infections. Paclitaxel induces hours after ingestion and may be associated with bronchospasm and a type 1 hypersensitivity reac- facial flushing, rhinorrhea, angioedema, and con- tion in up to 30% of patients. These examination; (5) absence of finger clubbing or patients will often present with dyspnea, tachy- subcutaneous nodules; (6) the presence of blood pnea, altered mental status, and a chest radiograph eosinophilia, proteinuria, or liver dysfunction; (7) revealing diffuse alveolar infiltrates. In general, prompt resolu- diagnosis is suspected to enhance renal clearance tion occurs with drug withdrawal, and rarely, a and thereby reduce the serum salicylate level. Hemodialysis is reserved for patients with aspirin- Methotrexate: See the section “Chemotherapy- associated seizures, refractory acidosis, coma, or Associated Pulmonary Toxicity ” for a discussion. Out- Penicillamine: Penicillamine is an antiinflam- come is generally favorable in young patients with matory, antifibrotic, and copper-chelating agent an acute salicylate overdose. The multiple medical problems and a long-term history manifestations of penicillamine-induced pulmo- of the ingestion of salicylates, and they have a more nary toxicity include the following: (1) interstitial subtle presentation. Bronchiolitis obliterans, in the presence A subset of patients present with a hypersensitiv- or absence of organizing pneumonia, occurs ity-type reaction associated with peripheral blood less frequently. As by gold therapy can be distinguished from the with gold therapy, it can be challenging to distin- patient’s underlying rheumatoid lung disease by guish drug-induced pulmonary toxicity from the the following: (1) an acute onset of dyspnea and patient’s underlying collagen vascular disorder. Lung biopsy specimens monary fibrosis, loosely formed granulomatous from these patients reveal bronchiolar constriction inflammation, pleural effusions, increased size of caused by mononuclear inflammation and fibrosis. Less com- patients die, whereas the remainder have very poor monly, fluoroquinolones, tetracycline, erythromy- quality of life due to a severe permanent residual cin, nitrofurantoin, isoniazid, paraaminosalicylic obstructive impairment. Penicillamine rarely induces Goodpasture There are no known risk factors, and most reactions syndrome, which consists of diffuse alveolar hem- are idiosyncratic. Typically, the patients present orrhage and rapidly progressive glomerulonephri- during a period of 1 to 4 weeks (can be delayed up tis caused by autoantibodies directed against to 1 year) with minimal, nonspecific respiratory components of the alveolar and glomerular base- complaints. There are case reports of this withdrawal perhaps with a short course of corti- syndrome occurring after penicillamine was used costeroids and antihistamines. The incidence of nitrofurantoin-induced and corticosteroids, the mortality rate is nearly adverse pulmonary effects is not firmly estab- 50%, and there is a high incidence of progression lished. As reviewed elsewhere,57 several theories 334 Drug-Induced Lung Diseases (Kamp) that are not mutually exclusive have been impli- a lung mass, or pleural effusions may be seen. Amiodarone is an iodine-containing phos- may reveal high-attenuation areas caused by pholipase inhibitor that causes lipid accumulation the iodine present in amiodarone. The management of amiodarone-induced pul- Uncommon reactions include hypersensitivity monary toxicity includes drug withdrawal and the pneumonitis, alveolar hypoventilation, and bron- initiation of a new antiarrhythmic agent or implan- chospasm. A trial of corticosteroids is often used in dyspnea with radiographic evidence of asymmet- symptomatic patients, but the efficacy of steroids ric chronic pneumonitis/fibrosis and an elevated has not been established. If amiodarone is the only inhibitor-induced angioedema includes drug effective agent in a patient with life-threatening withdrawal, attention to airway patency and, if arrhythmias, the dose must be reduced to the severe, the subcutaneous injection of epinephrine minimum that is effective (ideally 400 mg/d) (0. The mechanism underlying this serious adverse Statins: Statins are the most widely prescribed effect is unknown, but immune pathways, increased lipid-lowering drug primarily because of their well- tissue levels of bradykinin or histamine, and/or a documented beneficial effect on cardiovascular 336 Drug-Induced Lung Diseases (Kamp) morbidity and mortality. The chest radiographic and mental status, miotic pupils, and a chest radio- abnormalities include bilateral patchy ground-glass graph demonstrating perihilar alveolar infiltrates opacities and interstitial infiltrates. Statin-induced pneumonitis Management centers on supportive care including may become more commonly observed when used mechanical ventilation, which is needed in 40%. The term crack refers to the used, the route of administration, and the pre- popping sound that occurs when cocaine crystals senting clinical syndrome helps to narrow the broad are heated. Free-base crack cocaine smoking causes a distinct Noncardiac Pulmonary Edema: Noncardiac pul- set of pulmonary abnormalities that are termed monary edema is an infrequent complication of crack lung. Management centers on sup- by the Valsalva maneuver that is performed to portive care, and therapy with high-dose cortico- enhance alveolar-capillary cocaine absorption. The nodules may coalesce in a manner simi- uterol, terbutaline, ritodrine, isoxuprine, and sal- lar to that seen in silicosis, resulting in progressive butamol, are -adrenergic3 agents that are used massive pulmonary fibrosis with surrounding to inhibit uterine contractions during premature cysts and bullae. The mechanism of pulmonary edema has noncaseating giant-cell granulomatous infiltrates not been established but is believed to be caused containing birefringent talc crystals. The poor outcome tone normalizes, thereby promoting fluid move- noted in most patients is generally not altered by ment into the extravascular spaces, including the therapy with corticosteroids. Patients typi- cally present during or within 12 h of delivery Miscellaneous Agents (rarely beyond 12 h postpartum) with an acute onset of dyspnea, cough productive of pink- Contrast Media: Both the ionic and nonionic tinged sputum, chest pain, tachycardia, tachy- forms of contrast media can induce bronchospasm pnea, hypoxemic respiratory failure, and diffuse and a reduction in airflow. Contrast media rarely induces poten- ing: gastric acid aspiration, cardiac pulmonary tially fatal leukostasis in the pulmonary arterioles edema, pulmonary embolism, amniotic fluid and capillaries. Drug therapy: suppressive agent that is used in organ-transplant treatment of asthma with drugs modifying the leu- patients in the presence or absence of cyclosporine. Venous of bleomycin-induced epithelial cell apoptosis and thromboembolic disease and combined oral con- lung fibrosis by captopril or by a caspase inhibi- traceptives: results of international multicentre tor. Pulmonary of bleomycin-induced pulmonary fibrosis after function in patients receiving long-term low-dose adenovirus-mediated transfer of the bacterial bleo- methotrexate. Methotrex- shock, and multiple-system organ failure: A pseu- ate pneumonitis: bronchoalveolar lavage findings dosepsis syndrome associated with chronic salicy- suggest an immunologic disorder. Methotrexate pneumo- disease: clinical features, outcome, and differentia- nitis in rheumatoid arthritis: potential risk factors; tion from rheumatoid lung disease. Non-cardiogenic pulmonary Med 1997; 42:231–268 oedema after intravenous administration of non- An excellent overview of the area emphasizing the pulmo- ionic contrast media. Ann Intern Med 1989; A detailed analysis of the characteristic pathologic changes 110:714–718 associated with drug-induced adverse pulmonary effects that 84. Ann Intern Med 1997; 127:356– 364 Annotated Bibliography A multicenter, case-control study demonstrating the stron- gest clinical predictors for lung injury. Chest Chest Med 2004; 25:53–64 1991; 100:1391–1396 A succinct review of adverse pulmonary effects from new and A concise review of acute and chronic salicylate toxicity.

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The classical complement pathway requires activation by circulating antibodies cheap sominex online, IgM or IgG (specific immune response) buy sominex 25mg overnight delivery, while the alternative and lectin pathways can be activated in the absence of antibody (non-specific immune response) order sominex online from canada. C3 is first cleaved and activated, then causes a cascade of further activation events. C3b promotes opson- isation, C5a is a chemotactic protein, C3a and C5a trigger degranulation of mast cells and C5b initiates the membrane-attack pathway. The classical, lectin and alternative pathways converge into a final common pathway when C3 convertase (C3 con) cleaves C3 into C3a and C3b. As there are redundancies in the immune system, many complement disorders are never diagnosed. Hereditary angioedaema (also known as ‘Quincke oedaema’) is characterised by local swelling in subcutaneous tissues. It does not respond to antihistamines, corticosteroids or adrenaline (epinephrine). The cells ‘kill’ by releasing small cytoplasmic granules of proteins called perforin and granzyme, which cause the target cell to die by apoptosis or necrosis. Natural killer cells, along with macrophages and several other cell types, express the Fc receptor that binds the Fc portion of antibodies. It is one of the mechanisms through which antibodies, as part of the humoral immune response, can act to limit and contain an infection. There is an important immunological distinction between ‘apoptosis’ and cell ‘lysis’. For example, lysis of a virus-infected cell will only release virions to spread infection, whereas apoptosis leads to the death of the cell and the contained pathogen. Infants have passive immunity because they acquire antibodies through the placenta from the mother; these antibodies disappear at between 6 and 12 months of age. Passive immunisation involves transfusion of antiserum, containing antibodies formed in another person or animal; it provides immediate protection against an antigen, but does not provide long-lasting protection. Gamma globulin and equine (horse) tetanus antitoxin are examples of passive immunisation. B-cell lymphocytes, produced in the stem cells of the bone marrow, synthesise and release antibody; they oversee the humoral immune response. T-cell lymphocytes, produced in the bone marrow but sensitised in the thymus, are the basis of the cell-mediated immune response. Each B-cell has a unique membrane- bound immunoglobulin that will bind to a specific antigen. Once a B-cell encounters its cognate antigen and receives an additional signal from a T-helper cell, it can further differentiate (via clonal expansion; Figure 15. Prior to that expansion, it may undergo an intermediate differentiation step, leading to class switching; for example, synthesis of IgM antibody might be switched to IgG antibody. Therefore the anti- bodies produced by a particular clone can recognise and/or bind the same components (epitope) of a given antigen. The great diversity in immune response comes about because there are up to 109 clones, which recognise that many different antigens; the phenomenon of immunogenic memory relies on this clonality of B-cells. Activated B-cells, after an initial lag, produce highly specific (monoclonal) antibodies at a rate of up to 2000 molecules per second, over four to five days. They are soluble proteins secreted by the plasma offspring (clones) of activated B-cells. Short-lived cells that undergo apoptosis once the inciting agent has been eliminated. Memory B-cells Formed from activated B-cells that are specific to the antigen encountered in the primary immune response. Long-lived cells that can respond quickly following a second exposure to the same antigen. They express IgM in greater quantities than IgG and their receptors show polyspecificity, meaning that they have low affinities for many different antigens, but have a preference for other immunoglobulins, self-antigens and common bacterial polysaccharides. Present in low numbers in the lymph nodes and spleen, but found predominantly in the peritoneal and pleural cavities. Follicular B-cells A readily distinguished subtype, organized into the primary follicles of B-cell zones focused around follicular dendritic cells in the white pulp of the spleen and the cortical areas of peripheral lymph nodes. A small region at the tip of the protein is extremely variable, allowing millions of antibodies with slightly different tip structures to exist; this region is known as the hypervariable region. This huge diversity of antibodies allows the immune system to recognise an equally wide diversity of antigens. The blood constituents of gamma globulin are: IgG-76%, IgA-15%, IgM-8%, IgD-1% and IgE-0. IgG is the only antibody that can cross the placental barrier to the foetus, and it is responsible for the 3–6 month passive immunity of newborns that is conferred by the mother. The only antibody capable of crossing the placenta to give passive immunity to the foetus. Eliminates pathogens in the early stages of B-cell-mediated (humoral) immunity before there is sufficient IgG. The upper part, Fab (antigen binding) portion of the antibody molecule attaches to specific regions on the protein antigen, called epitopes. The Fc (crystallisable) region is responsible for effector functions; that is, the end to which immune cells can attach. IgM is the dominant antibody produced in primary immune responses, while IgG dominates in secondary immune responses. B-cells recognise their cognate antigen in its native form; they recognise free (soluble) antigen in the blood or lymph through their membrane-bound immunoglobulin. They secrete chemicals called lymphokines which stimulate cytotoxic T-cells and B-cells to grow and divide, attract neutrophils and enhance the ability of macrophages to engulf and destroy microbes. Lymphokines are cytokines, secreted by helper T-cells in response to stimulation by antigens, which act on other cells of the immune system. They belong to a sub-group of T-lymphocytes that are capable of inducing the death of infected somatic or tumour cells and cells that are infected with viruses (or other pathogens), or are otherwise damaged or dysfunctional. The strategy of T- and B-cell interaction with antigens is summarised in Figure 15. Pathogen Immature helper & Immature B-cells killer T-cells Engulfed by In thymus In bone marrow macrophage Peptide fragments of Mature inactive helper Mature inactive B-cells Free antigen in blood pathogen presented on & killer T-cells surface of antigen presenting cell (macrophage) Helper & killer T-cells activated by antigen If B-cell recognises antigen, it is activated, with presenting macrophage (if T-cells recognises the help of T-helper cell presented antigen) Helper T-cell activates B-cell Active helper & killer T-cells, Active B-cell including formation of memory undergoes clonal cells expansion, secretes killer T-cells require antibodies to bind helper T-cells for antigen activation Antibody binds antigen Memory B-cells (”tagging”) respond to subsequent infection by that antigen Memory T-cells can killer T-cells attack any Complement system Phagocytic cells engulf respond to subsequent cell infected with that destroys antigen tagged antigen infection by that antigen antigen Figure 15. Between α1andα2 is the peptide-binding groove, which binds peptides derived from cytosolic proteins. The groove consists of eight β-pleated sheets on the bottom and two α-helices making up the sides.

A wide range of patient sominex 25mg with mastercard, illness buy generic sominex 25mg on-line, and treatment variables increase the likelihood of developing delirium but pre-existing cognitive impairment order 25mg sominex mastercard, age extremes, and exposure to particular medications are particularly robust predictors of delirium across populations. The interaction between predisposition (baseline vulnerability) and precipitating insults account for delirium incidence. Inouye and Charpentier (1996) developed a model of 4 common predisposing and 5 precipitating factors that predicted a 17-fold variation in delirium risk in elderly medical patients. Baseline vulnerability is especially important such that minor insults can precipitate delirium in those with multiple predisposing factors. Aetiology Single-aetiology delirium is the exception with typically 3-4 significant causative factors relevant over the course of any single episode. It is thus important to remain vigilant to the possibility of multiple aetiological factors and to constantly re-evaluate throughout a delirium episode. Despite the many possible aetiological factors that contribute to delirium, the clinical presentation is remarkably consistent suggesting that delirium is a unitary syndrome reflecting a final common neural pathway for multiple diverse causes and pathophysiologies (Trzepacz ea, 2007). The prevailing neurochemical theory for delirium posits a relative imbalance of dopaminergic and cholinergic systems and is supported by evidence from preclinical studies, causation of delirium by agents that impact upon these neurochemical systems, and evidence for the effectiveness of dopamine blockers in delirium treatment. Current research is increasingly focusing upon inflammatory mechanisms, disruptions to the stress axis and disturbed oxidative metabolism as possible mechanisms in delirium pathogenesis (Trzepacz ea, 2007). Course and outcomes The course of delirium is highly variable reflecting the heterogeneity of aetiology and patient populations in which delirium occurs, with many recent studies emphasizing that it is frequently not the benign and transient condition that was previously thought. While in many cases delirium is brief (hours to days), represents a transitional state from unconsciousness or is a benign reaction to treatment exposures, in other cases it can be more prolonged or associated with serious complications and persistent cognitive difficulties where differentiation from dementia becomes difficult (MacLullich ea, 2009). Moreover, in the elderly, reduced post 950 hospital independence and elevated 1-year mortality rates occur. A recent study found that the risk of mortality increased by 11% for each additional 48 hours of active delirium (González ea, 2009). Other work has highlighted how experiencing an episode of delirium can accelerate the course of a pre-existing dementia (Fong ea, 2009). Importantly, these adverse outcomes are independent of factors such as age and severity of physical morbidity and are predicted by the presence and severity of delirium itself. Management The multifactorial nature of delirium means that optimal management requires the collaborative efforts of primary treating physicians and nursing staff with delirium specialists. Treatment is focused upon addressing the underlying aetiological causes as well as controlling delirium symptoms. Family and loved ones can assist in detection of changes in behaviour and mental state (‘not themselves’) and provide information about baseline cognitive and adaptive functioning and risk factor exposure. Common elements include elimination of unnecessary medications, careful attention to hydration and nutritional status, pain relief, correction of sensory deficits, sleep enhancement, early mobilisation, and cognitive stimulation. Recent studies of pharmacological prophylaxis of delirium indicate that use of small doses of haloperidol (Kalisvaart ea, 2005), olanzapine (Larsen ea, 2007), risperidone (Prakanrattana & Prapaitrakool, 2007) and melatonin (Al-Aama ea, 2010) can reduce the incidence of delirium in high risk populations. The pharmacological management of delirium has been poorly studied and although there are over 20 prospective studies of antipsychotic agents, well designed placebo-controlled studies remain lacking. Existing evidence suggests that more than two-thirds of treated delirious patients experience clinical improvement, typically within a week (Meagher & Leonard, 2008). There is little evidence to suggest differences in effectiveness for typical vs atypical agents (Hua ea, 2006), although the few randomised placebo-controlled trials have focused on the use of quetiapine (Tahir ea, 2010; Devlin ea, 2010). Treatment response includes improved cognitive and non-cognitive symptoms of delirium and does not appear to be closely linked to antipsychotic effect or sedative action. Both pharmacological and non-pharmacological strategies appear less effective in patients with concomitant dementia perhaps reflecting the inherently poor outcome of elderly demented populations with high physical comorbidity. There are concerns regarding the small but increased risk of cerebrovascular events in demented patients chronically receiving neuroleptics, but the relative risks of short-term use in delirium must be proportionalised against potential benefits. Occurrence and outcome of delirium in medical in-patients: a systematic literature review. A double-blind, randomized, placebo-controlled study of perioperative administration of olanzapine to prevent postoperative delirium in joint replacement patients. Academy of Psychosomatic medicine 54th Annual meeting proceedings,Kalisvaart Prakanrattana U, Prapaitrakool S. Drug-related Polypharmacy Drug / alcohol dependence Psychoactive drug use Specific agents (e. The neuropathogenesis of delirium involves dysfunction of brain regions and circuitry which may ultimately result in characteristic symptoms of delirium despite a wide variety of aetiologies and pathophysiological insults to the brain. It is often recurrent but the first episode is likely to be associated with a stressful life event. However, it is not recognized frequently nor treated adequately in this age group and the clinical picture may vary to a greater or lesser extent from that seen in younger adults and is often complicated by co-morbid dementia and physical illness. In addition, the loneliness associated with loss of a spouse and other social difficulties contribute in making elderly people more vulnerable to depression. Aetiology 955 In most cases it is difficult to isolate a single cause as many factors come into play to determine a person’s susceptibility for depression. Therefore, the term risk factors are used to describe some situations that could predispose a person to develop depression in later life. The most important risk factors for depression in later life are (Rodda ea, 2008): 1. Genetic predisposition: though it remains somewhat significant, the genetic risk of developing depression in later life is thought to be less than that of adolescents or younger adults. Physical illness: This accounts for a large proportion of depression in the elderly. Although there are certain diseases that are known to be associated with an increased risk, any debilitating illness can lead to the development of depression in older persons. The disease conditions with the greatest risk of depression include: - Cardiovascular disease, mainly myocardial infarction (25% have minor depression and 25% have major depression) and hypertension. Neurotransmitter theory: there is evidence to show that depression is closely linked to depletion of neurotransmitters such as serotonin and noradrenaline. Social isolation, deprivation and stressful life event: loneliness and lack of companionship especially that of a confiding one possibly due to bereavement is significantly associated with late onset depression. Low socioeconomic status, role transition like retirement and increased dependency due to frailty and poor physical health are also contributory factors. Vulnerable Personality: anxious and dependent personality disorders increase the vulnerability of certain elderly people to depression and are also poor prognostic indicators. Other associated symptoms which may be present depending on the severity include: -altered sleep pattern leading to early morning waking (>2 hours before normal)* -reduced appetite sometimes leading to weight loss of up to 5% or more body weight in past month* -diminished concentration and attention -low self-esteem and self confidence -feelings of guilt and worthlessness -negative view of the future which may sometimes border on hopelessness -anxiety and irritability -loss of libido* -motor agitation or retardation* -decreased emotional reactivity* -thoughts of self harm, passive death wish or active suicidal ideation. Co-occurrence of up to 4 of the symptoms marked with asterisk constitutes a somatic syndrome.

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Expiratory muscle weakness impairs with aminosteroid agents (pancuronium and the cough reflex discount sominex 25 mg mastercard, promoting retention of secretions vecuronium) discount sominex 25 mg online, in which renal excretion of active and pneumonia generic sominex 25 mg visa. Respiratory muscles may become these patients generally have intact sensation, weak as the result of denervation, myopathy, and usually have greater creatine kinase levels, and endocrinopathies. This complication is severe abnormalities in serum potassium, most common in patients who are receiving high magnesium, and phosphate, may interfere with. Denervation Myopathy Respiratory Muscles Muscular dystrophy Polymyositis The respiratory muscles perform the work of Drug-induced (neuromuscular blocking agents, corticosteroids) breathing. The diaphragm is the most important Endocrinopathy (hyperthyroidism, Cushing syndrome) inspiratory muscle, responsible for 60 to 90% of Metabolic work of breathing at rest. Contraction of the costal Hypokalemia component displaces abdominal viscera down- Hyperkalemia ward and lifts the lower rib cage; the crural com- Hypophosphatemia ponent displaces abdominal viscera downward. Hypomagnesemia Hypermagnesemia The external intercostals, scaleni, and sternocleido- Acidosis mastoids comprise the accessory muscles of inspi- Hyperinflation. When acidosis impairs the contractile fatigue is probably a consequence of reflex inhibi- force of respiratory muscles, a positive feedback tion, influenced by afferent and cortical signals, loop of respiratory muscle weakness and respira- perhaps endogenous opioids. It occurs when energy restores them to normal length, and the proportion demands on contracting muscles exceed the energy of slow-twitch muscle fibers increases. The efficiency of inspiratory muscle contraction In clinical practice, the strength of respiratory is impaired by lung volume, the presence of neu- muscles usually is measured with maximal pres- romuscular disease, and malnutrition. Body posi- sures at the mouth against a closed airway (maxi- tion also influences contractile efficiency; inspiration mum inspiratory pressure, maximum expiratory requires less effort in the upright position because pressure). The “gold standard” measurement, used the abdominal contents are displaced downward more in scientific investigations than in clinical by gravity, unloading the diaphragm. This is especially true measured with a gastric balloon catheter, and pleu- for patients with massive obesity, when assuming ral pressure measured in the esophagus. Fatigue is defined as a reduced capacity to The energy supply to muscles varies directly generate an expected force, which is corrected with with blood flow. It may be occurs because pulmonary edema increases the motivational when strength can be restored by work of breathing, and impaired hemodynamic voluntary effort and nonmotivational when strength function reduces blood flow to the respiratory is not restored by increased effort but the muscle muscles. Respiratory alternans, the alternating recruitment The interplay of increased work of breathing and derecruitment of the diaphragm and other and diminished respiratory drive is a prominent inspiratory muscles, often precedes the onset of feature of the obesity-hypoventilation syndrome paradoxical abdominal motion with respiration. If the underlying 45 mm Hg) during wakefulness in the absence condition that provoked muscle fatigue is not read- of other known causes of alveolar hypoventila- ily reversible, the patient will require mechanical tion. Similarly, drive in response to hypercapnia and hypoxemia, the role of strength and endurance training of the possibly related to decreased circulating levels or respiratory muscles has been under investigation receptor hyporesponsiveness to leptin, a hormone for decades, but there is still no good evidence to that acts on the hypothalamus to suppress appe- support its use. Obesity-related upper airway narrow- ing, dependent atelectasis, and excessive loading Excessive oxygen administration may worsen of respiratory muscles may all be contributing preexisting hypercapnia, especially in patients factors. Chest 2000; tive to increments in Paco2; and (3) the Haldane 117:205–225 effect, in which oxygen releases co2 bound to Review of the physiology of each component of the integrated hemoglobin, increasing Paco2. Am J Respir Crit Care Med 2003; 168:10–48 Severe kyphoscoliosis, obesity, thoracoplasty, Very thorough review of the role of respiratory muscles in and pleural thickening all may cause hypoventila- acute respiratory failure; specific neuromuscular diseases; tion by one of two general mechanisms, which can and the influence of chest wall, systemic diseases, and sur- be categorized as “can’t breathe” and “won’t gery on respiratory muscle function. N Engl J Med 1989; 321:1223–1231 134 Hypercapnic Respiratory Failure (Rosen) Concise summary of mechanisms, specific disorders, and These articles are cited because they are relatively current therapeutic strategies. Clin Infect Dis 2000; 31:1018–1024 failure in tetanus: case report and review of a 25-year The upsurge in diagnoses have been attributed to subcutane- experience. Chest 2001; 153:1686–1690 119:926–939 Muscle weakness occurred in 20 of 69 patients who received Reviews respiratory muscle physiology, evaluation of muscle both a neuromuscular blocking agent and corticosteroids dysfunction, and disorders that lead to prolonged ventilator compared with none of the 38 patients who received corti- dependency. N paralysis, and the incidence of weakness was not reduced in Engl J Med 1982; 307:786–797 patients who received atracurium compared with those who Develops the concept of “pump failure,” reviewing the phys- received pancuronium or vecuronium. Chest 2008; 134:867–870 between resting hypercapnia and physiologic param- Concise review with table summarizing the differential diag- eters before and after lung volume reduction surgery nosis of neuromuscular diseases that cause respiratory failure. As the cuff pressure • Review the current methods for evaluation of solitary exceeds the capillary pressure, blood supply to the pulmonary nodule tracheal mucosa is compromised. Tracheobronchomalacia This chapter is divided into six broad sections: (1) evaluation of the nonneoplastic diseases of Tracheobronchomalacia is a condition defined the tracheobronchial tree, (2) lobar atelectasis, by excessive expiratory collapse of the trachea and (3) evaluation of mediastinal structures and patho- bronchi. The Saber-sheath trachea is characterized by etiologies include infection, malignancy, trauma, marked decrease in the transverse diameter of the collagen vascular disease, and idiopathic entities intrathoracic trachea associated with an increase such as amyloidosis and tracheobronchopathia in its sagittal diameter. In summary, diagnosis of the nonneoplastic Relapsing polychondritis is a rare inflamma- diseases of the tracheobronchial tree requires tory disease that affects the cartilages of the ear, knowledge of the anatomy, and observation of the nose, respiratory tract, and joints. Amyloidosis is a rare condition characterized The differential diagnosis can be significantly by deposition of insoluble protein in the extracel- narrowed once the above questions have been lular tissues. Deposits within the tracheobronchial tree lead to Atelectasis is defined as decrease in volume of concentric or nodular thickening of the tracheal lung or a portion of the lung. Resorptive atelectasis is the most common type and results Wegener Granulomatosis from absorption of gas from the alveoli when the communication between the alveoli and the tra- It is a necrotizing granulomatous vasculitis that chea is obstructed by an endobronchial lesion or a involves the upper and lower respiratory tract. Passive atelectasis is caused by extrin- Involvement of the lung parenchyma shows mul- sic pressure on the lung from a large pleural effu- tiple nodules with or without cavitation. The exact mechanism ferential thickening, ulceration, and luminal nar- of adhesive atelectasis is poorly understood but is rowing of the trachea are noted. It is usually seen in patients with respira- Mounier-Kuhn syndrome tory distress syndrome and in those who are recov- (Tracheobronchomegaly) ering from surgery. Tracheobronchomegaly, also referred to as The most common cause of lobar atelectasis is Mounier-Kuhn syndrome, is a rare condition charac- obstruction by a central endobronchial lesion. On the frontal radiograph, a Primary and secondary signs on chest radiograph triangular opacity is visualized in the paraspinal help identify the atelectasis and site of endobron- location of the lower hemithorax, while on the lateral chial obstruction. The major sign of lobar atelec- projection, increased opacity overlying the lower tasis is opacification of the affected lobe due to thoracic vertebral bodies and loss of visualization airlessness and displacement of the interlobar of the posterior left hemidiaphragm are noted. Secondary signs of atelectasis include displacement of the mediastinal structures, eleva- Right Middle Lobe Atelectasis tion of the hemidiaphragm, decrease in the dis- tance of the intercostals spaces, displacement of On the frontal chest radiograph, the right the hila, and compensatory overinflation of the middle lobe collapse shows a vague opacity in the remaining lung. On the frontal chest radiograph, the right Rounded Atelectasis upper lobe collapses superiorly and medially, cre- ating a wedge-shaped opacity in the upper right It is an unusual form of passive atelectasis that hemithorax. The pleural fibrosis causes folding of the carcinoma may produce a characteristic appear- adjacent lung parenchyma that appears as a focal, ance on the frontal chest radiograph, termed the rounded opacity. On the lateral projec- rounded opacity with associated pleural thicken- tion, the collapsed lobe may appear as a triangular ing, “comet-tail” sign, and volume loss of the opacity with its apex at the hilum and its base at affected lobe are noted. Sometimes, the or unrecognized because of the nonspecific nature resultant overinflation of the superior segment of of its symptoms, signs, and laboratory test find- the left lower lobe inserts between the apex of the ings. The cardiac findings include right- single breath hold from the lung apices to the level sided chamber enlargement and right ventricular of the diaphragm. They include the anatomic pitfalls include lymph nodes, pulmonary following: (1) anterior mediastinum, which veins, impacted bronchi, and volume averaging of includes the retrosternal clear space and cardio- pulmonary arteries. On the computer workstation, phrenic angle; (2) the middle mediastinum, which if one scrolls in and out from the main pulmonary includes the retrosternal clear space, subcarinal artery, following each of the lobar, segmental, and region, and retrocardiac clear space; and (3) pos- subsegmental arteries, it is impossible to mistake terior mediastinum.